Zdenek Vrozina Profile picture
Mar 12 19 tweets 3 min read Read on X
Even in the Omicron era, long COVID remained common. A preprint meta-analysis showing that the burden persisted, even as the symptom profile shifted.🧵
This study is interesting because it does not just ask how common long COVID is. It looks at two things at the same time.
Which SARS-CoV-2 variant caused the infection, and how long after infection symptoms were assessed.
They included 35 studies with a total of about 159,000 people. Overall, long COVID showed up in about 28.5% of cases. It was more common after pre-Omicron infections, where the prevalence was around 35.5%, than after Omicron infections, where it was about 22.8%!
What also stands out is that nearly 30% of cases still had symptoms more than 6 months later.
Even more importantly, the symptom pattern itself seems to shift depending on the variant. Pre-Omicron infections were more strongly linked with shortness of breath and loss of smell, while Omicron was more associated with brain fog and paresthesia.
One of the key findings from the paper is that neurotropism appears to persist into the Omicron era. Long COVID did not disappear, and neurological and cognitive symptoms remained a prominent part of its presentation, even as the broader symptom profile evolved across variants and over time.
One very consistent finding was that fatigue remained the most common symptom across variants and across follow-up periods. Other frequent symptoms included brain fog, shortness of breath, and sleep problems.
Another striking point is that when the authors compared people assessed within 6 months versus after 6 months, the overall prevalence did not really drop much. About 27.3% vs 29.9%.
So at the level of pooled data, there was no clear sign that long COVID simply fades away with time. That matters, because it pushes back against the assumption that most people will automatically recover if they just wait long enough.
The symptom profile also seemed to evolve over time. In the earlier period, symptoms such as sleep disturbances, headache, and to some extent skin-related symptoms were more common. In longer follow-up, malaise and difficulty swallowing became more prominent.
The authors suggest this could reflect later-developing systemic or autonomic effects, meaning long COVID may be more than just the tail end of an acute infection. It may actually change form over time!
The highest overall prevalence appeared in people with pre-Omicron infections assessed within 6 months, at around 42.4%. The lowest was in Omicron cases assessed within 6 months, at around 18.5%. But the symptom patterns were quite distinct.
Early pre-Omicron cases had more sleep problems and headaches,
longer-term pre-Omicron cases had more shortness of breath, smell loss, runny nose, malaise, eye symptoms, nausea, and swallowing difficulties,
while early Omicron cases showed more brain fog and paresthesia.
That may be the most compelling finding of the whole paper. Pre-Omicron long COVID seems more respiratory and sensory, while Omicron-related long COVID looks more neurocognitive and systemic.
This could matter clinically! Follow-up and care might need to be more targeted depending on which variant likely caused the infection.
The paper challenges the idea that long COVID is a fixed syndrome. Instead, the authors describe it as a dynamic and heterogeneous condition, shaped by viral evolution, host immunity, and time since infection.
Yes, the study has some limitations. A lot of the data came from self-reported symptoms, which can introduce bias. In many studies, the variant was not confirmed by genomic sequencing, but inferred from the time period in which infection occurred.
Lugtu at al., Prevalence of Post-COVID Symptoms Across Variants of Concern and Follow-up Periods: A Systematic Review and Meta-Analysis. ijidonline.com/article/S1201-…
@szupraha @ZdravkoOnline @adamvojtech86 @adamkova_vera

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More from @ZdenekVrozina

Apr 7
Another piece of the puzzle. Post-COVID changes are not just an isolated problem affecting a few unlucky individuals. They appear to have consequences at the population level🧵
A striking headline from Austria - 4 in 10 people report smell or taste problems.
That figure comes from a new cross-sectional survey of 2340 adults in Austria, Germany, and Switzerland looking at self-reported smell and taste disorders after the COVID era.
The key point is that this was not mainly about complete smell loss.
The most commonly reported problems were olfactory intolerance, phantosmia, and parosmia - in other words, abnormal, distorted, or intrusive smell experiences.
Read 12 tweets
Apr 7
The Karaviti study is finally in print, which makes this a good time to revisit it. It shows that subclinical myocardial injury in children after COVID-19 may not be something exceptional🧵
The key point is often missed. This was not mainly a comparison of children with Long Covid versus children without Long Covid. It compared
children after COVID-19
healthy controls without prior SARS-CoV-2 exposure
In that comparison, conventional echocardiographic measures did not differ significantly, but the post-COVID group showed worse left ventricular global longitudinal strain (LV GLS).
Read 13 tweets
Apr 6
This study suggests a possible mechanism for how SARS-CoV-2 could harm neurons in the inner ear.
Not mainly through inflammation, but potentially through a more direct effect on spiral ganglion neurons, involving disrupted mTOR signaling, abnormal stress granules, and eventually - apoptosis🧵
That matters because spiral ganglion neurons are not some minor supporting cells. They are the neurons - that carry sound information from the cochlea into the auditory pathway.
If they are damaged, the problem is not just in the ear. It affects the neural transmission of sound itself.
The authors try to map out an actual chain of events. In their model, infection - and especially spike related effects - seems to disturb the cell’s stress-response machinery.
Stress granules start accumulating abnormally, mTOR signaling drops, and the neuron is pushed closer to cell death.
Read 9 tweets
Apr 4
A new paper looks at shared molecular mechanisms between COVID-19 and Parkinson’s disease. It does not show that COVID causes Parkinson’s.
What it does ask is whether the two conditions share biologically meaningful pathways🧵
The authors identified 77 overlapping differentially expressed genes across COVID-19 and Parkinson’s datasets. The main signal points to inflammation-related pathways plus signs of dopaminergic neuron dysfunction!
Their main candidate is CHI3L1. In the single-cell analysis, CHI3L1 was especially elevated in astrocytes from severe COVID-19 brain tissue, which led the authors to propose an astrocyte - CHI3L1 - neuroinflammation axis as one possible explanation for why infection might worsen neurological outcomes.
Read 13 tweets
Apr 3
A new population based study from Stockholm sends a pretty troubling signal.
During follow-up, a cardiovascular event occurred in 20.6% of men and 18.2% of women with diagnosed long COVID.🧵
In the control group without long COVID, the numbers were much lower. 11.1% for men and 8.4% for women.
These were not mainly patients recovering from severe acute COVID or ICU stays. The study focused on non-hospitalized adults aged 18-65 with no prior cardiovascular disease!
Read 14 tweets
Apr 2
A new 2026 paper looks at a possible mechanism behind rare myocarditis after COVID-19 mRNA vaccination.
Not vaccines broadly damage the heart.
More like
some people may be biologically more vulnerable than others🧵
The paper’s central idea is mitochondrial vulnerability.
In simple English
your mitochondria can seem mostly fine under normal conditions, but still handle stress badly when the system gets pushed.
That matters because this study is trying to explain a rare adverse event, not argue that this is happening across the whole population.
That distinction is everything.
Read 25 tweets

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